February 1991
Volume 32, Issue 2
Free
Articles  |   February 1991
Heterogeneous induction of major histocompatibility complex class II antigens on corneal endothelium by interferon-gamma.
Author Affiliations
  • B J Foets
    Department of Ophthalmology, University of Leuven, Belgium.
  • J J van den Oord
    Department of Ophthalmology, University of Leuven, Belgium.
  • A Billiau
    Department of Ophthalmology, University of Leuven, Belgium.
  • J Van Damme
    Department of Ophthalmology, University of Leuven, Belgium.
  • L Missotten
    Department of Ophthalmology, University of Leuven, Belgium.
Investigative Ophthalmology & Visual Science February 1991, Vol.32, 341-345. doi:
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      B J Foets, J J van den Oord, A Billiau, J Van Damme, L Missotten; Heterogeneous induction of major histocompatibility complex class II antigens on corneal endothelium by interferon-gamma.. Invest. Ophthalmol. Vis. Sci. 1991;32(2):341-345.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

The expression and distribution of major histocompatibility complex (MHC) class II gene products, HLA-DR, HLA-DQ, and the HLA-DR invariant chain, were studied on flat mounts of human corneal endothelial cells (HCEC) after in vitro incubation of donor corneas with interferon-gamma (IFN-gamma), interleukin-1 (IL-1), and IL-6, using a sensitive immunoperoxidase technique with monoclonal antibodies. Control HCEC and endothelium treated with IL-1 or IL-6 completely lacked MHC class II antigens. After treatment with 50 U/ml, 100 U/ml, 500 U/ml, and 5000 U/ml of human IFN-gamma, a mosaic-like, patchy staining for all MHC class II products was observed: part of the HCEC showed membranous and/or cytoplasmic positivity; other endothelial cells were negative. In addition, a dose-dependent response to IFN-gamma was observed: the proportion of cells expressing class II products rose with increasing doses of IFN-gamma. The induction of MHC class II antigen expression on HCEC by IFN-gamma was completely inhibited by the addition of a neutralizing antibody directed to IFN-gamma but not by IL-1 beta. The significance of these findings with respect to corneal transplantation immunology is discussed.

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